Hyponatremia in secondary adrenal insufficiency

[1nycdoc8]

I was wondering if someone could help explain to me why you would see hyponatremia in secondary adrenal insufficiency (deficient production of ACTH by the pituitary). The Z. glomerulosa is not controlled by ACTH so aldosterone should still be doing its thing right? Is it dilutional or something? Thanks for the help!

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[hartbot]

2 guesses from me:

1) deficient acth will cause atrophy of adrenal glands and eventually lead to decreased aldosterone

2) ACTH stimulates desmolase to lead off the first process of all the hormones from the adrenal cortex

 

[illixir]

I'm not even sure that secondary adrenal insufficiency is that common. Most common is tertiary from steroid use. And usually adrenal insufficiency is talked about with regards to Addison's which is where there is an infection or autoimmune process causing disruption to the whole gland. On histology, they are different cell types in the three layers though which presumably might have different receptors. Usually when adrenal insufficiency is secondary it's because of problems affecting the entire pituitary so that gives a more complex picture.

 

[SeeThroughMD]

Loss of ACTH --> loss of Cortisol --> loss of inhibitory feedback on ADH --> mild SIADH --> hyponatremia. (According to Goljan under table of clinical findings in hypopituitarism.)

 

[turkeyjerky]

Loss of ACTH --> loss of Cortisol --> loss of inhibitory feedback on ADH --> mild SIADH --> hyponatremia. (According to Goljan under table of clinical findings in hypopituitarism.)

yeah. guys--hyponatremia in adrenal insufficiency isn't due to loss of aldosterone. remember, the RAAS regulates total body sodium, not plasma osmolarity. the siadh you see in addison's is due to loss of cortisol which leads to increased adh (via two mechanisms: increased CRH which is an ADH secretagogue, as well as decreased effective arterial blood volume which leads to non-osmotic stimulation of ADH. The first mechanism is more impt).

This is why, whenever you suspect SIADH, you always need to rule out addison's and hypothyroidism.

 

[FutureDoc4]

"yeah. guys--hyponatremia in adrenal insufficiency isn't due to loss of aldosterone. remember, the RAAS regulates total body sodium, not plasma osmolarity.
the siadh you see in addison's is due to loss of cortisol which leads to increased adh (via two mechanisms: increased CRH which is an ADH secretagogue,
as well as decreased effective arterial blood volume which leads to non-osmotic stimulation of ADH. The first mechanism is more impt)."

Okay, source, or it didn't happen. I have never heard of CRH as a stimulus for ADH. And it doesnt make physiological sense....ADH is made in the hypothalamus and stored in the posterior piturary... because it's made in the hypothalamus it just seems unlikely it would be regulated by other hypothalamic releasing factors (at the same level)... things are regulated by levels high and higher up the "chain".

As far as I know, the only stimulus of ADH is change in plasma osmolarity.

 

[turkeyjerky]

"yeah. guys--hyponatremia in adrenal insufficiency isn't due to loss of aldosterone. remember, the RAAS regulates total body sodium, not plasma osmolarity.
the siadh you see in addison's is due to loss of cortisol which leads to increased adh (via two mechanisms: increased CRH which is an ADH secretagogue,
as well as decreased effective arterial blood volume which leads to non-osmotic stimulation of ADH. The first mechanism is more impt)."

Okay, source, or it didn't happen. I have never heard of CRH as a stimulus for ADH. And it doesnt make physiological sense....ADH is made in the hypothalamus and stored in the posterior piturary... because it's made in the hypothalamus it just seems unlikely it would be regulated by other hypothalamic releasing factors (at the same level)... things are regulated by levels high and higher up the "chain".

As far as I know, the only stimulus of ADH is change in plasma osmolarity.

Really? I'm surprised you didn't learn about this is school.

UptoDate article on Hyponatremia and hyperkalemia in adrenal insufficiency:

"The hypersecretion of ADH seen in cortisol deficiency may be in part due to the reductions in systemic blood pressure and cardiac output induced (via an unknown mechanism) by the lack of cortisol. However, a more important mechanism may be that ADH is an ACTH secretagogue, the secretion of which is stimulated by corticotropin releasing hormone (CRH) from the paraventricular nuclei in the hypothalamus [5-8]. Cortisol feeds back negatively on CRH and therefore ADH, an inhibitory effect that is removed with adrenal insufficiency [5,9]. It is unclear if the action of cortisol on ADH release is direct or is mediated by changes in the secretion of CRH"

 

[username456789]

Oddly, we were just "told" in school that ADH and CRH both stimulated ACTH release from corticotrophs, but with no explanation as to why ADH did (and certainly no explanation about the interaction between CRH and ADH).

Yay education.

 

[illixir]

That's ridiculous. A connection between cortisol and ADH has never come up for me in any of first 2 years, Robbins, UWorld, Kaplan, Goljan, DIT or FA. That's alot of sources for it to never have been mentioned once. (I don't know about that goljan table, I guess it's so easy for a small finding to be overlooked in that book) That really is what I hate about this test, there's always something else that's not written in any of the major texts that they'll put on your exam.

 

[Orbo]

I've never heard of this relationship between ADH and CRH, either. Like, whoa.

 

[FutureDoc4]

Wow, I had never heard of this in physio in undergrad/med school, in daddy robbins, Uworld, USMLERx, NOWHERE.....some of this information is so random.

 

[DrTacoElf]

ACTH, a pituitary peptide, also has some stimulating effect on aldosterone probably by stimulating the formation of deoxycorticosterone, a precursor of aldosterone.